Activation of endogenous retroviruses during brain development causes an inflammatory response
(2021) In EMBO Journal 40(9). p.106423-106423- Abstract
Endogenous retroviruses (ERVs) make up a large fraction of mammalian genomes and are thought to contribute to human disease, including brain disorders. In the brain, aberrant activation of ERVs is a potential trigger for an inflammatory response, but mechanistic insight into this phenomenon remains lacking. Using CRISPR/Cas9-based gene disruption of the epigenetic co-repressor protein Trim28, we found a dynamic H3K9me3-dependent regulation of ERVs in proliferating neural progenitor cells (NPCs), but not in adult neurons. In vivo deletion of Trim28 in cortical NPCs during mouse brain development resulted in viable offspring expressing high levels of ERVs in excitatory neurons in the adult brain. Neuronal ERV expression was linked to... (More)
Endogenous retroviruses (ERVs) make up a large fraction of mammalian genomes and are thought to contribute to human disease, including brain disorders. In the brain, aberrant activation of ERVs is a potential trigger for an inflammatory response, but mechanistic insight into this phenomenon remains lacking. Using CRISPR/Cas9-based gene disruption of the epigenetic co-repressor protein Trim28, we found a dynamic H3K9me3-dependent regulation of ERVs in proliferating neural progenitor cells (NPCs), but not in adult neurons. In vivo deletion of Trim28 in cortical NPCs during mouse brain development resulted in viable offspring expressing high levels of ERVs in excitatory neurons in the adult brain. Neuronal ERV expression was linked to activated microglia and the presence of ERV-derived proteins in aggregate-like structures. This study demonstrates that brain development is a critical period for the silencing of ERVs and provides causal in vivo evidence demonstrating that transcriptional activation of ERV in neurons results in an inflammatory response.
(Less)
- author
- organization
-
- MultiPark: Multidisciplinary research focused on Parkinson´s disease
- Molecular Neurogenetics (research group)
- StemTherapy: National Initiative on Stem Cells for Regenerative Therapy
- Wallenberg Neuroscience Centre, Lund
- Stem Cell Center
- Developmental and Regenerative Neurobiology (research group)
- Division of Molecular Medicine and Gene Therapy
- Targeted therapies in leukemia (research group)
- Division of Clinical Genetics
- WCMM-Wallenberg Centre for Molecular Medicine
- publishing date
- 2021
- type
- Contribution to journal
- publication status
- published
- subject
- in
- EMBO Journal
- volume
- 40
- issue
- 9
- pages
- 106423 - 106423
- publisher
- Oxford University Press
- external identifiers
-
- scopus:85101832411
- pmid:33644903
- ISSN
- 1460-2075
- DOI
- 10.15252/embj.2020106423
- language
- English
- LU publication?
- yes
- id
- 01956095-bde8-48fb-8ad2-a7955c2d8692
- date added to LUP
- 2021-05-05 09:30:51
- date last changed
- 2024-11-03 01:22:22
@article{01956095-bde8-48fb-8ad2-a7955c2d8692, abstract = {{<p>Endogenous retroviruses (ERVs) make up a large fraction of mammalian genomes and are thought to contribute to human disease, including brain disorders. In the brain, aberrant activation of ERVs is a potential trigger for an inflammatory response, but mechanistic insight into this phenomenon remains lacking. Using CRISPR/Cas9-based gene disruption of the epigenetic co-repressor protein Trim28, we found a dynamic H3K9me3-dependent regulation of ERVs in proliferating neural progenitor cells (NPCs), but not in adult neurons. In vivo deletion of Trim28 in cortical NPCs during mouse brain development resulted in viable offspring expressing high levels of ERVs in excitatory neurons in the adult brain. Neuronal ERV expression was linked to activated microglia and the presence of ERV-derived proteins in aggregate-like structures. This study demonstrates that brain development is a critical period for the silencing of ERVs and provides causal in vivo evidence demonstrating that transcriptional activation of ERV in neurons results in an inflammatory response.</p>}}, author = {{Jönsson, Marie E and Garza, Raquel and Sharma, Yogita and Petri, Rebecca and Södersten, Erik and Johansson, Jenny G and Johansson, Pia A and Atacho, Diahann Am and Pircs, Karolina and Madsen, Sofia and Yudovich, David and Ramakrishnan, Ramprasad and Holmberg, Johan and Larsson, Jonas and Jern, Patric and Jakobsson, Johan}}, issn = {{1460-2075}}, language = {{eng}}, number = {{9}}, pages = {{106423--106423}}, publisher = {{Oxford University Press}}, series = {{EMBO Journal}}, title = {{Activation of endogenous retroviruses during brain development causes an inflammatory response}}, url = {{http://dx.doi.org/10.15252/embj.2020106423}}, doi = {{10.15252/embj.2020106423}}, volume = {{40}}, year = {{2021}}, }